Voltage-sensitive conductances in dendrites of neurons have a fundamental influence on the processing of synaptic inputs. In the spinal motoneuron, active dendritic conductances play a major role in the generation of sustained depolarizations known as plateau potentials. The dendritic plateau potential results in potent amplification of synaptic current and can also cause bistable behavior. In a bistable cell, steady self-sustained firing can be evoked by a brief excitatory input and eliminated by a brief inhibition. Thus, the main role of synaptic input is to control the activation of the plateau and hence control the steady-state "excitability" of the dendritic tree. Furthermore, descending motor commands may control the amplitude of the dendritic plateau by adjusting the level of neuromodulatory drive to the spinal cord. This control suggests that motor commands might alter the synaptic integration in motoneurons to match the functional demands of different motor tasks. Our goal is to investigate the effects of dendritic plateau potentials on synaptic integration in motoneurons under different levels of neuromodulatory drive. All studies are done in an in vivo preparation, which provides a variety of well-characterized synaptic input systems and ample scope for altering descending neuromodulatory drive. Single electrode voltage clamp techniques are employed to measure the currents generated by the dendritic plateau potential. In Aim 1, we consider whether motoneurons can be bistable without descending neuromodulatory drive. Previous work has assumed that the monoamines serotonin and norepinephrine are the neuromodulators that are essential for expression of bistability. We investigate the possibility that sensory inputs acting on metabotropic glutamate receptors can generate bistable behavior even when complete spinal transection eliminates descending monoaminergic inputs. If so, then plateau potentials in motoneurons could contribute to the spasticity seen in spinal cord injury. Aim 2 investigates whether different neuromodulators generate exactly the same form of synaptic amplification and bistability. In Aim 3, we use a novel interpretation of our single electrode voltage clamp data to quantify the effects of dendritic plateau potentials on synaptic input. Aim 4 focuses on functional significance, using synaptic inputs to probe the firing behavior of bistable motoneurons. The results of the proposed experiments will provide a thorough understanding of the role of dendritic plateau potentials in both normal motor behavior and spinal cord injury.